Vestibulo-Autonomic Reflex and Monoamines

Abstract

Yates has reported that serotonin neurons in the raphe nuclei are associated with vestibulo-sympathetic responses and may possibly control BP changes during body replacement. Pompeiano demonstrated that the noradrenaline (NA) neurons in the locus coeruleus (LC) participate in posture control and modify the vestibulo-spinal reflex.
In our studies, LC-NA neuronal activity was inhibited by vestibular caloric stimulation, which causes vertigo clinically in humans. The vestibular input may be modified by the ventrolateral medulla (VLM) and then inhibit LC neuronal activity via GABAA receptors. Simultaneously, the VLM, the cardiovascular center in the brainstem, may change BP during vestibular stimulation. Thus, it is suggested that LC-NA inhibition is involved in the development of vertigo. Moreover, it is speculated that sopite syndrome, one of the major symptom complexes of motion sickness, is also evoked by LC-NA inhibition.
The central LC-NA and cholinergic neuron systems participate in vertigo and motion sickness, independent of the histaminergic neuron system. On the other hand, the cholinergic neuron system may mediate LC-NA inhibition during vestibulo-autonomic responses.
The LC-NA system projects to most higher centers and affects sensory information processing. Therefore, it is suggested that the suppression of the sensory information processing induced by LC-NA inhibition causes drowsiness, one of the major symptoms of vertigo and motion sickness. It is also speculated that LC-NA inhibition participates in the development of sensory mismatch.